We are primarily studying the effects of damage of arterioles and venules on the cerebral surface. Studies are of living, anesthetized animals. Only the vessel is injured, not the adjacent brain. Injury is produced by UV light acting upon the vessels. Injury is mediated by a circulating fluorescent dye, which acts as an energy absorbing target. Without the dye, no damage occurs. Damage produces platelet aggregation in situ. We study the capacity of drugs to interfere with this damage or to exacerbate it. This provides data concerning the possible prophylaxis of platelet aggregation in human cerebrovascular disease, particularly that involving damage to microvessels. In addition, the pharmacologic data provides insight into the mechanism underlying the platelet aggregation.